Anatomy and Physiology of the
Salivary Glands
The Major Salivary Glands
- Parotid
- Submandibular
- Sublingual
The Minor Salivary Glands
Anatomy: Parotid Gland
• Nearly 80% of the parotid
gland (PG) is found below the
level of the external auditory
canal, between the mandible
and the SCM.
• Superficial to the posterior
aspect of the masseter mm
• CN VII branches roughly divide the PG into superficial
and deep lobes while coursing anteriorly from the
stylomastoid foramen to the muscles of facial expression.
Anatomy: Parotid Duct
• Small ducts coalesce at the
anterosuperior aspect of the PG to
form Stensen’s duct.
• Runs anteriorly from the gland and
lies superficial to the masseter
muscle
• Follows a line from the EAM to a
point just above the commissure.
– Is inferior to the transverse facial
artery
– It is 1-3 mm in diameter
– 6cm in length
• At the anterior edge of the masseter muscle,
Stensen’s duct turns sharply medial and passes
through the buccinator muscle, buccal mucosa
and into the oral cavity opposite the maxillary
second molar.
Anatomy: Parotid Fascia
• Gland encapsulated by a fascial layer that is
continuous the deep cervical fascia (DCF).
• The stylomandibular ligament (portion of the
DCF) separates the parotid and submandibular
gland.
Parotid:
Parasympathetic Innervation
• Preganglionic parasympathetic (from CN9) arrives at otic
ganglion via lesser petrosal n.
• Postganglionic parasympathetic leaves the otic ganglion and
distributes to the parotid gland via the auriculotemporal nerve.
Parotid:
Sympathetic Innervation
• Postganglionic innervation is provided by the superior
cervical ganglion and distributes with the arterial system
Anatomy:
Submandibular gland
• Located in the submandibular triangle of the
neck, inferior & lateral to mylohyoid muscle.
• The posterior-superior portion of the gland
curves up around the posterior border of the
mylohyoid and gives rise to Wharton’s duct.
Anatomy:
Submandibular Duct
Wharton’s duct passes forward along the superior
surface of the mylohyoid adjacent to the lingual
nerve. Between Mylohyoid & Hyoglossus
5 cm in length ,2-4mm in diameter
Anatomy
Submandibular gland
• Innervation
– Superior Cervical Ganglion (symp)
– Submandibular Ganglion (para)
• Artery: Submental branch of Facial a.
• Vein: Anterior Facial vn.
• Lymphatics: Deep Cervical and Jugular chains
– Facial artery nodes
Submandibular
duct
Anatomy: Sublingual glands
Lie on the superior surface of the mylohyoid
muscle and are separated from the oral cavity by
a thin layer of mucosa.
The ducts of the sublingual glands are called
Bartholin’s ducts.
In most cases, Bartholin’s ducts consists of 8-20
smaller ducts of Rivinus. These ducts are short
and small in diameter.
Anatomy: Sublingual glands
•
•
•
•
•
•
Between Mandible & Genioglossus
No capsule
Ducts of Rivinus +/- Bartholin’s duct
Sialogram not possible
Innervation: Same as Submandibular
Artery/Vein: Sublingual branch of Lingual &
Submental branch of Facial
• Lymphatics: Submandibular nodes
Salivary Gland Infections
• Acute bacterial sialdenitis
• Chronic bacterial sialdenitis
• Viral infections
Sialadenitis represents inflammation
mainly involving the acinoparenchyma
of the gland.
Sialadenitis
Acute infection more
often affects the major
glands than the minor
glands1
Pathogenesis
1. Retrograde contamination of the salivary
ducts and parenchymal tissues by bacteria
inhabiting the oral cavity.
2. Stasis of salivary flow through the ducts
and parenchyma promotes acute
suppurative infection.
Acute Suppurative
• More common in parotid gland.
• Suppurative parotitis, surgical parotitis, postoperative parotitis, surgical mumps, and
pyogenic parotitis.
• The etiologic factor most associated with this
entity is the retrograde infection from the
mouth.
• 20% cases are bilateral7
Risk Factors for Sialadenitis
• Systemic dehydration (salivary stasis)
• Chronic disease and/or immunocompromise
–
–
–
–
–
–
Liver failure
Renal failure
DM, hypothyroid
Malnutrition
HIV
Sjögren’s syndrome
Risk Factors continued…
• Neoplasms (pressure occlusion of duct)
• Sialectasis (salivary duct dilation) increases
the risk for retrograde contamination. Is
associated with cystic fibrosis and
pneumoparotitis
• Extremes of age
• Poor oral hygiene
• Calculi, duct stricture
• NPO status (stimulatory effect of mastication on
salivary production is lost)
Acute Suppurative Parotitis - History
• Sudden onset of erythematous swelling of
the pre/post auricular areas extend into the
angle of the mandible.
• Is bilateral in 20%.
Bacteriology
• Purulent saliva should be sent for culture.
– Staphylococcus aureus is most common
– Streptococcus pnemoniae and S.pyogenes
– Haemophilus Influenzae also common
Lab Testing
• Parotitis is generally a clinical diagnosis
• However, in critically ill patients further diagnostic
evaluation may be required
• Elevated white blood cell count
• Serum amylase generally within normal
• If no response to antibiotics in 48 hrs can perform
MRI, CT or ultrasound to exclude abscess
formation
• Can perform needle aspiration of abscess
Treatment of Acute Sialadenitis
• Reverse the medical condition that may
have contributed to formation
• Discontinue anti-sialogogues if possible
• Warm compresses, maximize OH, give
sialogogues (lemon drops)
• External salivary gland massage if tolerated
Treatment of Acute
Sialadenitis/Parotitis
• Antibiotics!
• 70% of organisms produce B-lactamase or
penicillinase
• Need B-lactamase inhibitor like Augmentin or
Unasyn or second generation cephalosporin
• Can also consider adding metronidazole or
clindamycin to broaden coverage
Surgery for Acute Parotitis
• Limited role for surgery
• When a discrete abscess is identified,
surgical drainage is undertaken
• Approach is anteriorly based facial flap with
multiple superficial radial incisions created in
the parotid fascia parallel to the facial nerve
• Close over a drain
Chronic Sialadenitis
• Causative event is thought to be a lowered
secretion rate with subsequent salivary
stasis.
• More common in parotid gland.
• Damage from bouts of acute sialadenitis
over time leads to sialectasis, ductal ectasia
and progressive acinar destruction
combined with a lymphocyte infiltrate.
Chronic Sialadenitis
• Of importance in the workup…
• The clinician should look for a treatable
predisposing factor such as a calculus
or a stricture.
Acute viral infection (AVI)
• Mumps classically designates a viral
parotitis caused by the paramyxovirus
• However, a broad range of viral pathogens
have been identified as causes of AVI of
the salivary glands.
Viral Infections
As opposed to bacterial
sialadenitis, viral
infections of the
salivary glands are
SYSTEMIC from the
onset!
Virology
• Classic mumps syndrome is caused by
paramyxovirus, an RNA virus
• Others can cause acute viral parotitis:
– Coxsackie A & B, ECHO virus,
cytomegalovirus and adenovirus
• HIV involvement of parotid glands is a rare
cause of acute viral parotitis, is more
commonly associated with chronic cystic dz
Clinical presentation
• 30% experience prodromal symptoms prior
to development of parotitis
• Headache, myalgias, anorexia, malaise
• Onset of salivary gland involvement is
heralded by earache, gland pain,
dysphagia and trismus
Physical exam
• Glandular swelling (tense, firm) Parotid
gland involved frequently, SMG & SLG can
also be affected.
• May displace ispilateral pinna
• 75% cases involve bilateral parotids, may
not begin bilaterally (within 1-5 days may
become bilateral)….25% unilateral
• Low grade fever
Treatment
• Supportive
• Fluid
• Anti-inflammatories and analgesics
Complications
• Orchitis, testicular atrophy and sterility in
approximately 20% of young men
• Oophoritis in 5% females
• Aseptic meningitis in 10%
• Pancreatitis in 5%
• Sensorineural hearing loss <5%
– Usually permanent
– 80% cases are unilateral
Immunologic Disease
• Most common immunologic disorder
associated with salivary gland disease.
• Characterized by a lymphocyte-mediated
destruction of the exocrine glands leading
to xerostomia and keratoconjunctivitis sicca
Sjögren’s syndrome
• 90% cases occur in women
• Average age of onset is 50y
• Classic monograph on the disease published
in 1933 by Sjögren, a Swedish
ophthalmologist
Sjögren’s Syndrome
Two forms:
• Primary: involves the exocrine glands only
• Secondary: associated with a definable
autoimmune disease, usually rheumatoid
arthritis.
– 80% of primary and 30-40% of secondary
involves unilateral or bilateral salivary glands
swelling
Sjögren’s Syndrome
• Unilateral or bilateral salivary gland
swelling occurs, may be permanent or
intermittent.
• Rule out lymphoma
Sjögren’s Syndrome
• Keratoconjuntivitis sicca: diminished tear production
caused by lymphocytic cell replacement of the
lacrimal gland parenchyma.
• Evaluate with Schirmer test. Two 5 x 35mm strips of
red litmus paper placed in inferior fornix, left for 5
minutes. A positive finiding is lacrimation
of 5mm or less.
Approximately 85% specific & sensitive
Sjögren’s Treatment
• Avoid xerostomic meds if possible
• Avoid alcohol, tobacco (accentuates xerostomia)
• Sialogogue (eg:pilocarpine) use is limited by other
cholinergic effects like bradycardia & lacrimation
• Sugar free gum or diabetic confectionary
• Salivary substitutes/sprays
Sialadenosis
• Non-specific term used to describe a noninflammatory non-neoplastic enlargement of a
salivary gland, usually the parotid.
• May be called sialosis
• The enlargement is generally asymptomatic
• Mechanism is unknown in many cases.
Related to
a. Metabolic “endocrine sialendosis”
b. Nutritional “nutritional mumps”
a. Obesity: secondary to fatty hypertrophy
b. Malnutrition: acinar hypertrhophy
c. Any condition that interferes with the
absorption of nutrients (celiac dz, uremia,
chronic pancreatitis, etc)
Related to
a. Alcoholic cirrhosis: likely based on protein
deficiency & resultant acinar hypertrophy
b. Drug induced: iodine
c. Mumps
d. HIV
Granulomatous Disease
Primary Tuberculosis of the salivary glands:
– Uncommon, usually unilateral, parotid most
common affected
– Believed to arise from spread of a focus of
infection in tonsils
• Secondary TB may also involve the salivary
glands but tends to involve the SMG and is
associated with active pulmonary TB.
Sarcoidosis: a systemic disease characterized
by noncaseating granulomas in multiple
organ systems
• Clinically, SG involvement in 6% cases
• Heerfordts’s disease is a particular form of
sarcoid characterized by uveitis, parotid
enlargement and facial paralysis. Usually
seen in 20-30’s. Facial paralysis transient.
Cat Scratch Disease:
• Does not involve the salivary glands directly,
but involves the periparotid and
submandibular triangle lymph nodes
• May involve SG by contiguous spread.
• Bacteria is Bartonella Henselae(G-R)
• Also, toxoplasmosis and actinomycosis.
Sialolithiasis
• The exact pathogenesis of sialolithiasis remains unknown.
• Thought to form via….
an initial organic nidus that progressively grows by
deposition of layers of inorganic and organic substances.
• May eventually obstruct flow of saliva from the gland to the
oral cavity.
Acute ductal obstruction may occur at meal time when
saliva producing is at its maximum, the resultant
swelling is sudden and can be painful.
Gradually reduction of the swelling can result but it
recurs repeatedly when flow is stimulated.
This process may continue until complete obstruction
and/or infection occurs.
Etiology
•
•
•
•
•
Water hardness likelihood? …Maybe….
Hypercalcemia…in rats only
Xerostomic meds
Tobacco smoking, positive correlation
Smoking has an increased cytotoxic effect on saliva,
decreases PMN phagocytic ability and reduces salivary
proteins
Gout is the only systemic disease known to cause
salivary calculi and these are composed of uric
acid.
Stone Composition
• Organic; often predominate in the center
–
–
–
–
Glycoproteins
Mucopolysaccarides
Bacteria!
Cellular debris
• Inorganic; often in the periphery
– Calcium carbonates & calcium phosphates in the
form of hydroxyapatite
Reasons sialolithiasis may occur more
often in the SMG
• Saliva more alkaline
• Higher concentration of calcium and phosphate in
the saliva
• Higher mucus content
• Longer duct
• Anti-gravity flow
Other characteristics:
• Despite a similar chemical make-up,
80-90% of SMG calculi are radio-opaque7
50-80% of parotid calculi are radiolucent7
• 30% of SMG stones are multiple
60% of Parotid stones are multiple
Clinical presentation
• Painful swelling (60%)
• Painless swelling (30%)
• Pain only (12%)
– Sometimes described as recurrent salivary
colic and spasmodic pains upon eating
Diagnostics: Plain occlusal film
• Effective for
intraductal stones,
while….
• intraglandular,
radiolucent or
small stones may
be missed.
Diagnostic approach:
Diagnostic Sialendoscopy2
• Allows complete exploration of the ductal
system, direct visualization of duct
pathology
• Success rate of >95%2
• Disadvantage: technically challenging,
trauma could result in stenosis,
perforation
Sialolithiasis Treatment
• None: antibiotics and anti-inflammatories,
stone passage.
• Stone excision:
– Lithotripsy
– Interventional sialendoscopy
– Simple removal (20% recurrence)7
• Gland excision
•
•
•
•
hoping for spontaneous
If patients DO defer treatment, they need to know:
Stones will likely enlarge over time
Seek treatment early if infection develops
Salivary gland massage and hyper-hydration when symptoms
develop.
Transoral vs. Extraoral Removal
• Some say:
– if a stone can be palpated thru the mouth, it can be
removed trans-orally (TO)
– Or if it can be visualized on a true central occlusal
radiograph, it can be removed (TO).
– Finally, if it is no further than 2cm from the punctum,
it can be removed (TO).
Gland excision indicated
• Very posterior stones
• Intra-glandular stones
• Significantly
symptomatic patients
• Failed
transoral
approach